Pain Pathophys and Pharm Flashcards
What is the definition of Nociception?
Sensory detection of tissue damage or stimuli that can potentially damage tissue
What are the 3 Nociceptor Afferent Fibers? Describe each.
- C fibers:
- respond to thermal, mechanical, and chemical = polymodal; dull pain
- smallest unmyelinated, transmit at slowest speed
- A-delta:
- respond to intense mechanical and thermal, first sharp pain
- thinkly myelinated, transmit at fastest
- A-beta:
- respond maximally to light touch and may modulate pain
Pain modulation by Periaqueductal Gray (PAG) is stimulated by input from what 3 sources?
1) thalamus
2) hypothalamus
3) amygdala
What 2 sites does the Periaqueductal Gray activate? What do these do activated sites do?
Raphe nuclei:
- sends inhibitory enkephalinergic and serotonergic axons to dorsal horn (via dosrolateral funiculus) to inhibit pain transmission
Locus coeruleus:
- sends separate noradrenergic inhibitory axons
What usually causes visceral pain? How is it often described?
Usually caused by stretching of unmyelinated fibers that innervate the walls of organs
“crampy, dull or achy”
Where is visceral pain usually felt? Why is it poorly localized?
Intraperitoneal organs are bilaterally innervated, so visceral pain is independent of right or left anatomic origin.
What is parietal (somatic) pain?
Inflammation of parietal peritoneium; localized to dermatone superficial to the site of the painful stimulus
What is the definition of referred pain?
Pain localized in part of body that is remote from its source
What is the mechanism of referred pain?
Visceral afferent nerve fibers enter the spinal cord very close to input from sensory nerve fibers from skin or underlying muscle. Since there are more sensory nerve fibers and they are more strongly stimulated, the pain is perceived as coming from the skin or muscle.
3 common examples of referred pain (location and pain location)
location, pain location:
diaphragm, shoulder (but when you press on shoulder, you feel no pain)
heart, precordium and inner side of arm
ureter, testis
endogenous opioid peptides and their preferred receptor
- B endorphin
- Enkephalin
- Dynorphin
- B endorphin: mu
- Enkephalin: delta
- Dynorphin: **kappa **
opiates effect on decreasing pain [1(3), 1]
- inhibits ascending pathways of pain
- inhibits the presynaptic release and postsynaptic response to excitatory neurotransmitters (e.g. substance P)
- inhibits spinal cord transmission neurons
- inhibits activity in the thalamus
- activate descending inhibitory pathways
Toxicity of NSAIDs (4 areas)
KIDNEY:
- decreased kidney function in patients with decreased ECV or underlying kidney disease
- NA retention (prostaglandins natriuretic)
HEART:
- increased BP (average 5 mmHg) // Hypertension
PLATELET:
- nonselective reversible effect (COX2 no effect)
GI:
- ulceration (less with COX2)
- dyspepsia without ulceration
Opioids cause constipation which does not go away while on drug. What is the mechanisms?
mechanism: CNS effect, but mainly due to binding to mu2 opioid receptors in intestine
what is the treatment for constipation as a side effect of opioids? (3)
- prophylaxis with stimulant laxative (Senna) - do NOT wait for them to get constipated. start right away
- injectable methylnaltrexone for severe constipation
- oral alvimopan (mu antagonist)
